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Infection and Immunity, November 2004, p. 6694-6698, Vol. 72, No. 11
0019-9567/04/$08.00+0 DOI: 10.1128/IAI.72.11.6694-6698.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.
Timothy J. Mitchell,
Peter W. Andrew, and
Christopher O'Callaghan
Department of Infection, Immunity and Inflammation, University of Leicester, Leicester, United Kingdom
Received 2 April 2004/ Returned for modification 17 June 2004/ Accepted 22 July 2004
Ciliated ependymal cells line the ventricular surfaces and aqueducts of the brain. In ex vivo experiments, pneumolysin caused rapid inhibition of the ependymal ciliary beat frequency and caused ependymal cell disruption. Wild-type pneumococci and pneumococci deficient in pneumolysin caused ciliary slowing, but penicillin lysis of wild-type, not pneumolysin-deficient, pneumococci increased the extent of ciliary inhibition. This effect was abolished by antipneumolysin antibody. Ependymal ciliary stasis by purified pneumolysin was also blocked by the addition of antipneumolysin monoclonal antibodies. These data show that antibiotic lysis of Streptococcus pneumoniae can be detrimental to the ciliated ependyma and that antipneumolysin antibody may have a therapeutic potential.
Present address: Manor Hospital, Moat Rd., Walsall WS2 9PS, United Kingdom.
Present address: Division of Infection and Immunity, University of Glasgow, Glasgow G12 8QQ, United Kingdom.
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